Материал: MasterPass _ Pharmacology in 7 Days for Medical Students

PHARMACOLOGY IN 7 DAYS FOR MEDICAL STUDENTS

3Endocrine: Hyperglycemia (occurs with gatifloxacin).

4Joints: Reversible arthropathy and tendonitis.

5Allergic reactions: Photosensitivity.

Sulfonamides: therapeutic uses

1As topical agents: sulfonamides are used in trachoma and bacterial conjunctivitis; also in burn cases, sulfonamides are used as a prophylaxis against superadded infections.

2UTI.

3Ulcerative colitis.

4Enteritis.

5Rheumatoid arthritis.

6Dermatitis herpetiformis.

7Pneumocystis carinii pneumonia (Co-tromixazole).

8Resistant malaria (Fansidar – a combination of sulphadoxine + pyrimethamine).

9Acute toxoplasmosis (Fansidar).

Co-tromixazole: therapeutic uses

1Pneumocystis carinii pneumonia.

2H. influenzae.

3Streptococcus pneumoniae.

4Klebsiella pneumoniae.

5Moraxella catarrhalis.

6Non-tuberculous mycobacterial infections.

7GIT infections (like shigellosis, typhoid fever).

8UTI.

9Gonococcal urethritis.

Co-trimoxazole/sulfonamide: side effects

1 Hyper-sensitivity reactions:

a Common: Fever and skin rash.

bRare: Exfoliative dermatitis, polyarteritis nodosa (PAN) and Stevens-Johnson syndrome (SJS).

2GIT: N, V, D and elevation of hepatic aminotransferases.

3Hematotoxicity: Hemolytic anaemia (especially in patients with G6PD deficiency), aplastic anaemia, granulocytopenia and thrombocytopenia.

4Nephrotoxicity: Sulfonamides can precipitate in the acidic urine, in turn causing crystalluria and hematuria.

5Use in pregnancy: When used in third trimester, sulfonamides, by displacing bilirubin from the plasma proteins, allow free bilirubin to cross BBB and get deposited in fetal brain causing kernicterus.

6Important drug interactions: Sulfonamides compete with other drugs (like warfarin and methotrexate) for plasma protein binding. This in turn can transiently raise the levels of the said drugs.

Macrolides: therapeutic uses

1Alternative to penicillins in patients who are penicillin allergic/resistant.

2Atypical pneumonia due to mycoplasma pneumoniae and legionella.

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3Campylobacter jejuni infections.

4Chlamydial infections (UTI, trachoma, psittacosis).

5Diphtheria (caused by Corynebacterium diphtheriae).

6Whooping cough.

7Toxoplasmosis.

Macrolides: side effects

1GIT: When taken empty stomach, they can cause epigastric distress, NVD and abdominal pain by stimulating motilin receptors.

2Cholestatic jaundice: It occurs with erythromycin estolate, especially when used in pregnant ladies.

3Drug interactions: Both erythromycin and clarithromycin inhibit hepatic cytochrome P450 → ↓ metabolism of drugs being metabolised by this enzymatic system (e.g. anticoagulants, carbamazapine, digoxin and theophylline) → ↑ side effects. Azithromycin (because of its lactone ring structure) does not inhibit hepatic cytochrome P450 and thus it is free of above mentioned drug interactions.

4Blood dyscrasias: Eosinophilia and leukocytosis.

5Allergic reactions: Fever and skin rash.

6Intravenous administration can cause thrombophlebitis.

Amoebicides: therapeutic uses

1Amoebiasis d/t Entamoeba histolytica (both intestinal and hepatic).

2Giardiasis.

3H. pylori eradication.

4Trichomoniasis (both vaginal and urethral).

5Acute ulcerative gingivitis.

6Anaerobic infections (d/t Bacteroides fragilis).

7Abdominal surgery.

8Clostridial infection (like pseudomembranous colitis).

9Brain abscess.

10Indolent ulcers.

11Rosacea.

Amoebicides: side effects

If given for 3–5 days, only a few and mild side effects develop. Severe side effects only develop when amoebicides are given for up to 10 days.

1At injection site, pain, tenderness, muscle weakness and abscess formation can occur.

2Cardiotoxicity in the form of arrhythmias and CCF is rare.

3N, V (of central origin) and D.

4Generalised muscle weakness associated with tenderness, stiffness, tremors and mild paresthesias.

Atropine: therapeutic uses

1Before and during surgery:

•Before surgery/pre-anaesthetic medication: Almost half an hour before administering GA, atropine is given to prevent laryngeal spasm because it extensively decreases tracheobronchial secretions.

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•During surgery: To prevent reflex slowing or asystole due to handling of viscera in abdominal surgery.

2Motion sickness: It is given prophylactically before travelling because it has its effect on vestibular pathway.

3Parkinsonism: It is used to counteract excessive ACh effect when there is less dopamine.

4Ophthalmic Uses:

•To dilate pupil.

•To give rest to the eye in inflammatory conditions (nowadays adrenergic drugs are preferred for giving rest to eye).

•For measuring refractive error in children and in non-cooperative patients.

•For breaking adhesions in anterior and posterior synechiae. In such cases, atropine is given alternatively with miotics.

5Treatment of organophosphorous compound and mushroom poisoning.

6Antispasmodic for treating colicky abdominal pain.

7Antidiarrhoeal: It relaxes smooth muscles.

8Antisialagogue: It reduces salivary secretions.

9Bronchial asthma: It causes bronchodilatation.

10Nocturnal enuresis (bed-wetting) in children.

11Hyperhydrosis (excessive sweating).

12Treatment of bradycardia: In acute MI, hyperactive carotid sinus reflex and tightcollar syndrome.

Atropine: side effects

1Hyperthermia (‘atropine fever’): inhibition of sweating → ↓ heat loss from the body → fever. This is the most dangerous side effect of antimuscarinic drugs and is potentially fatal especially in infants. Atropine is relatively contraindicated in infants because of the danger of hyperthermia.

2‘Atropine flush’: At toxic doses, atropine can cause dilatation of the subcutaneous blood vessels causing the skin to appear ‘red’. This is called ‘atropine flush’ and is the diagnostic sign of toxicity with antimuscarinic drugs.

3‘Atropine madness’: At toxic doses, atropine can cause delirium, convulsions and hallucinations – called atropine madness. Central muscarinic receptors are probably involved.

4Pupillary dilatation → blurring of vision. Pupillary dilatation can also precipitate an acute attack of angle-closure glaucoma (atropine is relatively contraindicated in patients of angle-closure glaucoma).

5Dryness of mouth (d/t inhibition of salivation).

6Tachycardia → tachyarrhythmias may occur. At toxic doses, atropine can cause a paradoxical effect (i.e. blockade of intra-ventricular conduction).

7Constipation.

8Urinary retention, especially in elderly men with BPH. Atropine is relatively contraindicated in patients with BPH.

Pilocarpine: therapeutic uses

•For treatment of glaucoma (both closed-angle and wide-angle).

•To reduce the effect of mydriatics, e.g. atropine, homatropine and eucatropine.

•For the treatment of inflammatory conditions of the eye.

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•To break the adhesions b/w iris and lens (posterior synechiae) or iris and cornea (anterior synechiae). In such cases, it is used alternatively with mydriatics.

•In patients of Parkinsonism being treated with anticholinergic drugs like benzhexol.

•Xerostomia.

•Sjögren’s syndrome.

•Patients undergoing radiotherapy.

Note: It is not used for systemic diseases because it may lead to increase in tracheobronchial secretions and pulmonary oedema.

Physostigmine: therapeutic uses

1 Ophthalmic uses:

aAcute congestive glaucoma: Physostigmine and pilocarpine eye drops plus acetazolamide (orally or by injection) are used for the treatment of acute

congestive glaucoma. Just like pilocarpine, physostigmine lowers the IOP by improving the drainage of aqueous humour by its miotic effect.

b To counteract the mydriatics effect of homatropine.

cTo break the adhesions b/w lens and iris or iris and cornea (known as posterior and anterior synechiae, respectively). In such cases, it is used alternatively with the mydriatics like homatropine.

2It is the drug of first choice in cases of atropine poisoning. It is also recommended in cases of phenothiazines, antihistamines and TCA poisoning. Physostigmine being a tertiary amine can cross the BBB and reverse the toxic CNS effects of these drugs. Neostigmine, on the other hand, cannot do the same because being a quaternary amine, it cannot cross the BBB.

3Physostigmine can be of some help in patients of senile dementia and Alzheimer’s disease where there is deficiency of ACh in CNS due to loss of cholinergic neurons in memory pathway (septohippocampal pathway). If, however, physostigmine is given in very high doses, it can cause death by respiratory failure.

Neostigmine: therapeutic uses

1Relief of abdominal distension/paralytic ileus.

2Relief of urinary retention in bladder atonia.

3Relief of myasthenia gravis.

Differeces between Physostigmine and Neostigmine

LMNOP:

Lipid soluble Miotic Natural

Orally absorbed well Physostigmine

Neostigmine, on the contrary, is:

•Water soluble

•Used in myasthenia gravis

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•Synthetic

•Poor oral absorption

Neuromuscular (NM) blocking agents: therapeutic uses

1As adjuvant to anaesthesia.

2For rapid endotracheal intubation (suxamethonium is used).

3In crush injuries of chest (to provide rest to the respiratory muscles).

4With electroconvulsive therapy (ECT) in cases of severe depression (to prevent trauma).

5For diagnosis of myasthenia gravis.

6Treatment of poisoning due to convulsant drugs, e.g. strychnine.

7For treatment of tetanus and status epilepticus.

Suxamethonium: therapeutic uses

1For rapid endotracheal intubation.

2Short procedures (e.g. local surgeries, upper or lower GI endoscopy, ECT, etc.).

Acetazolamide: therapeutic uses

1Rarely used as a diuretic (limited efficacy).

2Glaucoma.

3Prevention and treatment of mountain sickness.

4Familial periodic paralysis.

5Petit-mal epilepsy.

6Correction of metabolic alkalosis (especially diuretics-induced).

Beta blockers: therapeutic uses

1 CVS:

a Antihypertensive (beta blockers → ↓ cardiac output and ↓ renin secretion). b Anti-arrhythmic.

c Ischaemic heart disease (angina and MI).

dChronic (not acute) heart failure: Beta blockers have been proved to reduce mortality in heart failure cases by some unknown mechanism.

e Hypertrophic obstructive cardiomyopathy (HOCM).

2 CNS:

a Migraine prophylaxis. b Familial tremors.

c Anxiety-related tremors.

3Thyroid: Thyrotoxicosis (Graves’ disease) and thyroid crisis.

4Eye: Glaucoma (β-blockers → ↓ secretion of aqueous humour).

5Abdomen:

a Portal hypertension.

b Pheochromocytoma: Treated by combined α and β-blocking agent (e.g. labetalol).

Beta blockers: side effects

1CNS:

•Insomnia, bad dreams, lassitude and depression. Beta blockers with low lipidsolubility and thus poor CNS penetration (e.g. atenolol, nadolol) produce only minimal CNS side effects.

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